Schizophrenia

Question 1

Schizophrenia

Answer 1

• Distorted thinking, faulty perception and attention, lack of emotional expressiveness, disturbances in behavior etc.
• Substance use, suicide, men more, culture differences (African Americans), beings in adolescence.

Question 2

Positive symptoms: Delusions (6)

Answer 2

Belief contrary to reality:
- Thought insertion
- Thought broadcasting
- External force controlling their thinking/behavior
- Grandiose delusions: importance, power, knowledge, identity
- Ideas of reference
- Persecutory delusions: danger beliefs

Question 3

Positive symptoms: Hallucinations

Answer 3

• Sensory experiences in the absence of any stimulation from environment
• Auditory more than visual
• During: Broca’s area (frontal cortex: producing speech) and wernicke’s (temporal: understanding speech) are active. Therefore: miscommunication between the frontal lobe and temporal lobes.

Question 4

Negative symptoms (5)

Answer 4

• Endure beyond an acute episode.
• Many negative symptoms = poor quality of life
  1. A-volition: lack of motivation.
  2. A-sociality: impairments in social relationships.
  3. Anhedonia: Loss of interest in please. Consummatory: experienced in the moment, anticipatory: pleasure from future events.
  4. Blunted effect: lack of outward expression of emotions
  5. Alogia: reduction in speech

Question 5

Disorganized speech

Answer 5

• Formal thought disorder: problems in organizing ideas and speaking coherently.
• Loose associations or derailment: successful in communication but difficulty sticking to one topic

Question 6

Disorganized behavior

Answer 6

• No ability to organize behaviors to conform to community standards.
• Catatonia: spectrum of unusual gestures or immobility or even waxy flexibility.

Question 7

Prevalence

Answer 7

• 1%
• Men more likely
• African Americans - bias
• Comorbidity - substance abuse
• Age: adolescents, not in children, later for women.

Question 8

Etiology: Behavioral genetics

Answer 8

1. Family studies: relatives = high risk, more negative symptoms, gene + environment/experiences
2. Twin studies: high risk
3. Adoption studies
4. Familial high-risk studies

Question 9

Etiology: molecular genetics research

Answer 9

• Not transmitted by a single gene - multiple genes
  1. DRD2: encodes specific type of dopamine receptor (d2)
  2. COMT: associated with cognitive control processes that rely on prefrontal cortex. Chromosome 22.
  3. CNV deletions: 1% of genetic variance.

Question 10

Etiology: dopamine theory

Answer 10

• High dopamine levels = SP
• Related with positive and disorganized symptoms.
• Dopamine abnormalities in the prefrontal cortex accounts for negative symptoms - no strong evidence.

Question 11

Etiology: other neurotransmitters

Answer 11

• Blocking D2 and 5HT2 (serotonin and dopamine)
• Little serotonin = too much dopamine = SP
• Low levels of glutamate found in cerebrospinal fluid.
• High levels of amino acid homocysteine which interacts with NMDA receptor.
• PCP and ketamine induce positive and negative symptoms by interfering with NMDA receptors.
• Decreases NMDA and low glutamate levels lead to SP and disorganized symptoms.

Question 12

Etiology: brain structures and functions

Answer 12

1. Enlarged ventricles
   - Loss of brain cells.
   - Correlated with impaired performance on neuro-psychological tests, poor functioning and poor response to medication.
2. Prefrontal cortex
   - Plays a role for speech, decision making, emotion, goal-direction etc.
   - MRI show reduction in gray matter and volume.
   - Lower glucose metabolism
   - Less activation related to severe negative symptoms
   - Dendritic spines are lost (not neurons) = disrupted connections between neurons = speech and behavioral disorganization symptoms. Link with CNV genes.
3. Temporal cortex
   - Temporal gyrus, hippocampus, insula, fusiform gyrus, amygdala and cingulate cortex.
   - Reducting in cortical gray matter and volume
   - HPA axis affected.

Question 13

Connectivity in the brain

Answer 13

• Less connectivity in brain white matter in the frontal/temporal cortices.
• Less connectivity in the brain networks, frontro-parietal and default mode networks = poor performance on cognitive tests.

Question 14

Etiology: environmental factors

Answer 14

1. Damage during gestation or birth: reduced oxygen - loss of cortical gray matter.
2. Maternal infections during pregnancy: toxoplasma gondii
3. Cannabis: worsens symptoms + increase onset.

Question 15

Etiology: sociocultural factors

Answer 15

• High poverty = SP
• Living in urbanc areas = SP
• Migration = SP (3x for first generation, 4x for second generation)

Question 16

Etiology: Family related factors

Answer 16

• High EE (critical comments + hostility + emotional over-involvement) influences relapse.
• Anglo-Americans higher EE than Mexican Americans
• High EE increases stress = activation HPA axis which increases dopamine levels.

Question 17

Etiology: retrospective studies

Answer 17

• Low IQ, more delinquent and withdrawn
• Boys rated disagreeable, girls rated as passive
• Young adults showed poor motor skills and expression of negative emotions
• Adults scored lower on IQ and other cognitive tests

Question 18

Etiology: prospective studies

Answer 18

• Low IQ before age 7 and consistent = Schizophrenia
• Social and academic difficulties predicted conversion to the disorder.

Question 19

Treatment for schizophrenia: medication (first generation)

Answer 19

• Reduce positive and disorganized symptoms, little effect on negative symptoms.
• 30% do not respond, 50% quit after 1y, 75% after 2y
• Maintenance dose: just enough to see therapeutic effect
  Side effects:
• Sedation, dizziness, parkinson’s symptoms, tremors, dystonia, akasthesia.

Question 20

Treatment for schizophrenia: medication (2nd generation)

Answer 20

• Work the same, but added advantage for positive symptoms.
• Equally effective but more effective for negative symptoms
• 75% stopped after 18m
  Side effects:
• Parkinson’s symptoms, weight gain, diabetes etc.

Question 21

Treatment for schizophrenia: psychosocial interventions + medications

Answer 21

• Skill training, cognitive behavior therapy, family based.
• Combining = low rates of relapse and discontinuations, improvements in functioning

Question 22

Treatment for schizophrenia: social skills training

Answer 22

• How to successfully manage a wide variety of interpersonal situations.
• Role playing, group exercises in therapy group and actual social situations.
• Reduces relapses, better social functioning and high quality of life.

Question 23

Treatment for schizophrenia: family therapy

Answer 23

• Education
• Information about antipsychotic meds
• Blame avoidance and reduction
• Communication and problem-solving skills within family
• Social network expansion
• Hope
• Effective at reducing relapse if lasts for 9 months.

Question 24

Treatment for schizophrenia: CBT

Answer 24

• Testing out delusional beliefs through discussions
• Reduces negative symptoms
• Combination of cbt + social skills = effective.
• NAVIGATE: other combination (medication + family psycho-education + individual therapy + employment and education) = effective for those who started early.

Question 25

Treatment for schizophrenia: cognitive remediation therapy

Answer 25

• Improves the fundamental aspects of cognition
• Hours of computer-based training in attention, memory, and problem solving.

Question 26

Treatment for schizophrenia: psycho-education

Answer 26

• Knowledge about their illness, symptoms, course of symptoms, biological + psychological triggers, treatment etc.

Question 27

Treatment for schizophrenia: residential treatment

Answer 27

• Alternative for those not well enough to live on their own/with families.
• Part time job/live regular lives before gradually returning to ordinary community life.